Exercise attenuates diabetes-induced ultrastructural changes in rat cardiac tissue
Exercise is an effective nonpharmacological treatment in the prevention of mortality and morbidity due to cardiovascular disease in Type I diabetes. This study sought to explore the effects of endurance exercise on the ultrastructural changes seen in diabetic cardiomyopathy. Seven-week-old rats were...
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Veröffentlicht in: | Medicine and science in sports and exercise 2004-11, Vol.36 (11), p.1863-1870 |
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Sprache: | eng |
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Zusammenfassung: | Exercise is an effective nonpharmacological treatment in the prevention of mortality and morbidity due to cardiovascular disease in Type I diabetes. This study sought to explore the effects of endurance exercise on the ultrastructural changes seen in diabetic cardiomyopathy.
Seven-week-old rats were divided into three groups consisting of sedentary nondiabetic control, sedentary diabetic, and exercised diabetic animals. Diabetes was induced using streptozotocin injection, and the exercised animals were run daily on a treadmill for 9 wk. Changes in heart ultrastructure were analyzed using transmission electron microscopy.
Ultrastructural changes in the left ventricle produced by diabetes included changes in myofibrillar arrangements, disrupted mitochondria, and increased cytoplasmic area with an increase in lipid amounts and an increase in individual collagen fiber cross-sectional surface area. Also, an increase in heterochromatin lining the nuclear envelope and an increase in invaginations of the nuclear membrane were observed in cardiomyocytes from diabetic rats when compared with the nuclei from nondiabetic cells. Exercise was found to significantly attenuate the diabetes-induced changes in collagen fibrils, cytoplasmic area, and level of mitochondrial disruption. In contrast, exercise did not appear to significantly influence myofibril volume density, lipid accumulation, or nuclear deformities.
These findings indicate that exercise restores specific ultrastructural characteristics of diabetic cardiomyopathy returning them toward nondiabetic phenotypes, particularly in the mitochondria and extracellular matrix proteins. |
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ISSN: | 0195-9131 |
DOI: | 10.1249/01.MSS.0000145461.38224.EC |